DETAILED ACTION
Notice of Pre-AIA or AIA Status
The present application, filed on or after March 16, 2013, is being examined under the first inventor to file provisions of the AIA . Claims 1-20, filed January 20, 2026 are currently pending.
Information Disclosure Statement
The information disclosure statement (IDS) submitted on 01/20/2026 is in compliance with the provisions of 37 CFR 1.97. Accordingly, the information disclosure statement is being considered by the examiner.
Response to Amendment
Applicant’s amendments, filed 01/20/2026 are acknowledged. Applicant has amended the scope of claim 14 to wherein the patient, prior to starting sotorasib therapy comprises an intracranial lesion that is greater than 10 mm.
Applicant's arguments, filed 01/20/2026 have been fully considered. Rejections and/or objections not reiterated from the previous Office Action are hereby withdrawn. The following rejections and/or objections are either reiterated or newly applied. They constitute the complete set of rejections and objections presently being applied to the instant application.
Claim Rejections - 35 USC § 103-Rejection Maintained
In the event the determination of the status of the application as subject to AIA 35 U.S.C. 102 and 103 (or as subject to pre-AIA 35 U.S.C. 102 and 103) is incorrect, any correction of the statutory basis (i.e., changing from AIA to pre-AIA ) for the rejection will not be considered a new ground of rejection if the prior art relied upon, and the rationale supporting the rejection, would be the same under either status.
The following is a quotation of 35 U.S.C. 103 which forms the basis for all obviousness rejections set forth in this Office action:
A patent for a claimed invention may not be obtained, notwithstanding that the claimed invention is not identically disclosed as set forth in section 102, if the differences between the claimed invention and the prior art are such that the claimed invention as a whole would have been obvious before the effective filing date of the claimed invention to a person having ordinary skill in the art to which the claimed invention pertains. Patentability shall not be negated by the manner in which the invention was made.
Claim(s) 1-12 and 15-20 are rejected under 35 U.S.C. 103 as being unpatentable over the combination of Hong (New England Journal of Medicine Vol. 383 pages 1207-1217. Published 9/2020), Canon (Nature Vol. 575 pages 217-223 published 2019) and Yamamoto (Journal of Thoracic Oncology Vol. 14 pages E97-E99 published 2019).
Claim 1 is directed to a method of treating a cancer having a KRAS G12C mutation in a human patient with active brain metastases, the method comprising administering to the human patient a therapeutically effective amount sotorasib, wherein the cancer having a KRAS G12C mutation is non-small cell lung cancer or colorectal cancer. The phrase “treating” is not defined in the present specification. As shown in [0070] of the specification, a response can be measured by one or more of decrease in tumor size. Given the broadest reasonable interpretation of the phrase “treating” and in view of the lack of definition of the phrase in the claim, the phrase embraces treating the primary KRAS G12C mutant non-small cell lung tumor or primary KRAS G12C mutant colorectal carcinoma tumor comprising the administration of a therapeutically effective amount of sotorasib reads on the claimed methodology as well as treating the active brain metastases developed from the primary tumors. In addition, the claim embraces the transitional phrase “comprising”. Applicant is reminded of MPEP 2111.03 wherein the transitional phrase “comprising” " is inclusive or open-ended and does not exclude additional, unrecited elements or method steps. See, e.g., Mars Inc. v. H.J. Heinz Co., 377 F.3d 1369, 1376, 71 USPQ2d 1837, 1843 (Fed. Cir. 2004). In the present case, the pending claims do not exclude the administration of unrecited elements, such as the MEK inhibitor trametinib, dabrafenib and radiation therapy with sotorasib.
Hong (New England Journal of Medicine Vol. 383 pages 1207-1217. Published 9/2020) Hong teaches that KRAS mutant metastatic non-small cell lung cancer and colorectal carcinoma patients do not benefit from standard anti-EGFR therapies and have poorer progression-free survival and overall survival compared to wild type KRAS patients (page 1216 left col). Hong teaches that considering the poor prognosis in patient with metastatic disease and the lack of effective treatments in this population, controlling tumor burden with oral therapies may be meaningful (page 1216 left col.). Hong teaches the method of treating metastatic KRAS G12C mutant non-small cell lung cancer and metastatic KRAS G12C colorectal carcinoma in a subject in need comprising orally administering sotorasib in doses ranging from 180 mg to 960 mg to said subject (abstract, page 1208 right col., page 1209 right col.).
As shown in Table 3, 35% of said metastatic non-small cell lung cancer patients treated with 960 mg of sotorasib yielded a tumor reduction and 91% of said patients comprised disease control (page 1213 left col.). In addition, 66% of said metastatic colorectal carcinoma patients comprised stabilized disease upon receiving 960 mg of sotorasib (page 1213, page 1215 right col., Table 3). As shown in Figure 1, doses ranging from 180 mg to 960 mg were effective at yielding tumor reduction in the afflicted neoplastic patient.
Regarding claims 15-20, metastatic patients previously treated with anti-PD-1 immunotherapies and platinum-based chemotherapies were embraced within the patient population treated with sotorasib (page 1209 right col.). All patients were previously treated with platinum-based chemotherapies (Table 1). Regarding the conditional language limitation wherein the patient also underwent treatment with an EGFR, ALK or ROS1 inhibitor if the cancer also exhibited a mutation in EGFR, ALK or ROS1, Hong is silent as to these mutations in the mutant KRAS G12C non-small cell lung cancer patient population. As such, treatment of said patients with sotorasib and who had previously been treated with platinum-based chemotherapies embodied within Hong reads on the limitations of claims 19-20.
Canon (Nature Vol. 575 pages 217-223 published 2019) teaches the method of treating human patients comprising orally administering AMG-510 to KRAS G12C mutant non-small cell lung cancer.
As evidenced by paragraph [0011] of the instant specification, compound AMG-510 is art-recognized as sotorasib. As shown in Figure 3b, a significant reduction in tumor burden was achieved with the administered 360 mg dose. Regarding claims 15-16, said patients were previously treated with carboplatin and anti-PD-1 (nivolumab) prior to administration of compound AMG-510 (page 220 left col. Figure 3, Extended Data Figure 5). Canon also teaches that AMG-510 is synergistic with the MEK inhibitor trametinib inhibiting KRAS G12C non-small cell cancer tumor growth (NCI-H373) and KRAS G12C colorectal cancer tumor growth (pages 220-221; Figure 4a).
The difference between the methodologies of Hong and Canon and that of the present claims is that neither Hong nor Cannon specifically teaches treating said KRAS G12C mutant non-small cell cancer patient wherein the KRAS G12C metastatic non-small cell lung cancer patient treated with sotorasib comprises active brain metastases.
Yamamoto (Journal of Thoracic Oncology Vol. 14 pages E97-E99 published 2019) teaches treating non-small cell lung cancer patients with active brain metastases comprising administration of a therapeutically effective amount of trametinib and dabrafenib along with radiation therapy. As shown in Figures 2-3, Yamamoto teaches that said trametinib-dabrafenib-radiation regimen is efficacious for the treatment of non-small cell lung cancer with intracranial metastases.
Therefore, one of ordinary skill in the art of treating KRAS G12C mutant metastatic non-small cell lung cancer and metastatic colorectal carcinoma, knowing that administration of sotorasib is efficacious at treating metastatic KRAS G12C mutant non-small cell lung cancer and colorectal cancer in a subject in need as taught by Hong, coupled with the knowledge that sotorasib is synergistic with the MEK inhibitor trametinib in reducing KRAS G12C non-small cell lung cancer and KRAS G12C colorectal tumor burden as taught by Canon, said skilled artisan would have found it prima facie obvious to administer sotorasib in combination with the MEK inhibitor trametinib, dabrafenib and radiation therapy to treat KRAS G12C non-small cell lung cancer and KRAS G12C colorectal carcinoma patients with active brain metastases in view of Yamamoto.
Motivation to administer the MEK inhibitor trametinib, radiation therapy and dabrafenib in combination with the art-recognized KRAS G12C mutant non-small cell lung cancer and colorectal cancer treating sotorasib of Hong and Canon to KRAS G12C mutant non-small cell lung cancer and colorectal cancer patients with active brain metastases logically flows from the fact that Yamamoto teaches that trametinib, radiation therapy and dabrafenib combination is efficacious at inhibiting growth of non-small cell lung cancer patients with active brain metastasis. Considering that sotorasib is synergistic with the MEK inhibitor trametinib in reducing KRAS G12C non-small cell lung cancer and KRAS G12C colorectal tumor burden as taught by Canon, said artisan would have readily predicted that administration of the combination of sotorasib, the MEK inhibitor trametinib, radiation therapy and dabrafenib to the KRAS G12C mutant non-small cell lung cancer and colorectal cancer patients with active brain metastases would have effectively inhibited primary and metastatic tumor growth in the afflicted neoplastic patient and the active brain metastases. Reduction of the primary lung tumor hinders the capacity of the primary tumor to metastasize to the brain, thereby decreasing new tumor formation and treating the disease as recited in [0070] of the specification.
Regarding the limitation wherein the daily dose of sotorasib administered to the metastatic non-small cell lung cancer or colorectal carcinoma patient is 480 mg or 240 mg (claims 5-6, 8-9, 11-12), the optimum dose of sotorasib administered to the metastatic non-small cell lung cancer or colorectal carcinoma patient with active brain metastases would have been a matter well within the insight of one of ordinary skill in the art. Such a determination would have been made in accordance with a variety of factors, such as the route of administration, pharmacological considerations, such as activity, efficacy, pharmacokinetics and toxicology profiles of the combined regimen, as well as the age, weight, sex, diet and severity of the medical condition of the patient. Thus, the dosing of sotorasib that would have been employed would have varied widely and, in the absence of evidence to the contrary, the current claimed specific administration regimen is not seen to be inconsistent with one that would have been determined by the skilled artisan. Moreover, as shown in Figure 1 of Hong, doses ranging from 180 mg to 960 mg were effective at yielding tumor reduction in the afflicted neoplastic patient. Furthermore, absent and evidence demonstrating a patentable difference between the compositions administered and the criticality of the claimed frequency and dosing cycles, the determination of the optimum or workable frequency of administration given the guidance of the prior art would have been generally prima facie obvious to the skilled artisan. Please see MPEP 2144.05 [R-2](II)(A) and In re Aller, 220 F.2d 454, 456, 105 USPQ 233, 235 (CCPA 1955)(”[W]here the general conditions of the claim are disclosed in the prior art, it is not inventive to discover the workable ranges by routine experimentation.”)
Claim(s) 13-14 are rejected under 35 U.S.C. 103 as being unpatentable over the combination of Hong (New England Journal of Medicine Vol. 383 pages 1207-1217. Published 9/2020), Canon (Nature Vol. 575 pages 217-223 published 2019) and Yamamoto (Journal of Thoracic Oncology Vol. 14 pages E97-E99 published 2019) as applied to claims 1-12 and 15-20 in view of the combined teachings of Lin (Lancet Oncology Vol. 16 pages 270-278. Published 2015) and Cui (Lung Cancer Vol. 146 pages 310-317 published 2020).
As disclosed above, the combination of Hong, Canon and Yamamoto render obvious the method of treating mutant KRAS G12C non-small cell lung cancer and colorectal carcinoma patients further containing active brain metastases comprising administering a therapeutically effective amount of a combination comprising the art-recognized KRAS G12C inhibitor sotorasib in combination with trametinib, radiation therapy and dabrafenib. Motivation to administer the chemotherapeutic combination naturally flows from the fact that Yamamoto teaches that trametinib, radiation therapy and dabrafenib combination is efficacious at inhibiting growth of non-small cell lung cancer patients with active brain metastasis. As sotorasib is art-recognized as being synergistic with the MEK inhibitor trametinib in reducing KRAS G12C non-small cell lung cancer and KRAS G12C colorectal tumor burden as taught by Canon, said artisan would have readily predicted that administration of the combination of sotorasib, the MEK inhibitor trametinib, radiation therapy and dabrafenib to the KRAS G12C mutant non-small cell lung cancer and colorectal cancer patients with active brain metastases would have effectively inhibited primary and metastatic tumor growth in the afflicted neoplastic patient and the active brain metastases. Reduction of the primary lung tumor hinders the capacity of the primary tumor to metastasize to the brain, thereby decreasing new tumor formation and treating the disease as recited in [0070] of the specification.
However, the combination of Hong, Canon and Yamamoto does not specifically teach wherein the intracranial lesion of the active brain metastasis measures greater than 10 mm.
Lin (Lancet Oncology Vol. 16 pages 270-278. Published 2015) teaches assessment criteria for active brain metastases. Lin teaches that measurable disease is defined as a contrast-enhancing lesion that can be accurately measured in at least one dimension with a minimum size of 10 mm (page 271 left col.) Lin states that for studies wherein the CNS objective response is the primary endpoint, it is highly recommended that there is a cutoff of 10 mm to limit the study to measurable disease (page 271 right col.)
Cui (Lung Cancer Vol. 146 pages 310-317 published 2020) teaches mutant KRAS G12C metastatic non-small cell lung cancer patients and colorectal carcinoma patients comprising active brain metastases. Cui teaches that there is a poorer prognosis in both patient classes compared to KRAS wild type tumors (pages 310-311). Cui also teaches that there is a high incidence of KRAS mutant G12C non-small cell lung cancer developing brain metastatic lesions. Cui teaches that 28% of patients diagnosed with KRAS G12C metastatic non-small cell lung cancer comprise active brain metastases and that 40% of said KRAS G12C metastatic non-small cell lung cancer patients will develop active brain metastases during follow up (page 313-314). Cui teaches that in this distinct patient population, treatments with good intracranial penetration is important for long-term disease control (page 314 right col.).
Therefore, one of ordinary skill in the art of treating patients comprising mutant KRAS G12C non-small cell lung cancer and colorectal cancer and further comprising active brain metastases comprising administering a therapeutically effective amount of the art-recognized KRAS G12C inhibitor sotorasib in combination with trametinib, radiation therapy and dabrafenib as taught by the combination of Hong, Canon and Yamamoto above, said skilled artisan would have found it prima facie obvious to administer said sotorasib, trametinib, radiation therapy and dabrafenib therapeutic regimen to said KRAS mutant G12C non-small cell lung cancer patient or colorectal carcinoma patient with an metastatic cranial lesion of greater than 10 mm in view of Cui and Lin.
Considering Lin teaches that measurable disease of an active brain metastasis is defined as a contrast-enhancing lesion that can be accurately measured in at least one dimension with a minimum size of 10 mm, said skilled artisan would have readily predicted that administering the sotorasib, trametinib and dabrafenib regimen to a patient with an active brain metastasis includes a patient with measurable disease, and thus embraces a patient with a contrast-enhancing lesion that can be accurately measured in at least one dimension with a minimum size of 10 mm. Further, considering Cui teaches that there is a high incidence of KRAS mutant G12C non-small cell lung and colorectal cancer patients developing brain metastatic lesions along with poorer prognosis of said patients compared to wild type disease, said skilled artisan would have been motivated to administer the sotorasib, trametinib and dabrafenib regimen in order to improve the therapeutic outcome in the poorer prognosed patient class.
Applicant traverses. Applicant asserts that the independent claim should be interpreted as sotorasib for treating active brain metastasis in a cancer comprising a KRAS G12C mutation, wherein the cancer is either non-small cell lung cancer or colorectal carcinoma. Applicant asserts that in view of Amgen Inc. V. Sandoz Inc., 923F.3d 1023, 1031 (Fed. Cir. 2019) the administered therapeutically effective amount of a chemotherapeutic agent requires that the recited chemotherapeutic agent be administered to treat the underlying disease and thus the administered therapeutically effective amount is required to treat the active brain metastases. Because the prior art fails to provide a reasonable expectation of success for the treatment of active brain metastases by sotorasib, claim 1 is nonobvious for at least that reason.
Response to Arguments
Applicant’s arguments, filed 01/20/2026 are acknowledged and have been carefully considered. Regarding Applicant’s contention that the independent claim should be interpreted as sotorasib for treating active brain metastasis in a cancer comprising a KRAS G12C mutation, wherein the cancer is either non-small cell lung cancer or colorectal carcinoma, this argument is unavailing. As recited in MPEP 2173, the claim must be given its broadest reasonable interpretation consistent with the specification as it would be interpreted by one of ordinary skill in the art. Under the broadest reasonable interpretation, words of the claim must be given their plain meaning unless such meaning is inconsistent with the specification. In the present case, the phrase “treating” is not defined in the present specification. In paragraph [0070] of the specification, reduction of the primary lung tumor hinders the capacity of the primary tumor to metastasize to the brain, thereby decreasing new tumor formation and treating the disease.
In the present case, the way the claim is written, the limitation of “treating a cancer having a KRAS G12C mutation in a human patient with active brain metastases” limits the method to a distinct sub patient population being administered a therapeutically effective dose of sotorasib. The active brain metastases are a classification phenotype for the sub patient population with the underlying disease and are not required to be treated with the claimed chemotherapeutic agent. Rather, the underlying disease in the instant claims is a cancer having a KRAS G12C mutation in a human patient, wherein the cancer is non-small cell lung cancer or colorectal carcinoma, both of which are effectively treated with a therapeutically effective amount of sotorasib as shown in Hong and Canon above. In the instant case, there is no distinct limitation in the claim requiring that sotorasib “effectively reduces the active brain metastases”. Nor is the independent claim directed to a method of treating active brain metastases in a human subject wherein the human subject comprises non-small cell lung cancer or colorectal carcinoma, wherein the non-small cell lung cancer or colorectal carcinoma comprises KRAS G12C mutation, wherein the method comprises administering to the human patient a therapeutically effective amount of sotorasib. As such, given the broadest reasonable interpretation of the claim, the claim embraces the administration of a therapeutically effective amount of sotorasib to effectively treat the underlying disease of a primary KRAS G12C non-small cell tumor or primary KRAS G12C colorectal carcinoma in a human patient and not solely the treatment of the active brain metastases as Applicant suggests. Reduction of the primary lung tumor as recited in Hong and Canon above with said therapeutically effective amount of sotorasib hinders the capacity of the primary tumor to metastasize to the brain, thereby decreasing new tumor formation, which corresponds to yielding a positive response in the criteria of [0070] of the specification.
Applicant is further reminded of MPEP 2111.03 wherein the transitional phrase “comprising” is inclusive or open-ended and does not exclude additional, unrecited elements or method steps. See, e.g., Mars Inc. v. H.J. Heinz Co., 377 F.3d 1369, 1376, 71 USPQ2d 1837, 1843 (Fed. Cir. 2004). In the present case, the pending claims do not exclude the administration of unrecited elements, such as the MEK inhibitor trametinib, dabrafenib and radiation therapy with the sotorasib regimen to further inhibit intercranial metastatic growth in the afflicted neoplastic patient.
In the present case, the prior art of Canon and Hong explicitly teaches that a therapeutically effective amount of sotorasib is efficacious at inhibiting non-small cell lung cancer or colorectal cancer primary tumorigenesis in human patients with KRAS G12C mutant non-small cell lung cancer or colorectal cancer, wherein 35% of said metastatic non-small cell lung cancer patients treated with 960 mg of sotorasib yielded a tumor reduction and 91% of said patients comprised disease control while 66% of said metastatic colorectal carcinoma patients comprised stabilized disease upon receiving 960 mg of sotorasib (Hong page 1213 left col., page 1215, Table 3). It is also noted that Canon also teaches that sotorasib/AMG-510 is synergistic with the MEK inhibitor trametinib inhibiting KRAS G12C non-small cell cancer tumor growth (NCI-H373) and KRAS G12C colorectal cancer tumor growth (pages 220-221; Figure 4a).
Considering Yamamoto (Journal of Thoracic Oncology Vol. 14 pages E97-E99 published 2019) teaches that administration of a therapeutically effective amount of trametinib and dabrafenib along with radiation therapy is efficacious at treating active intracranial metastases in non-small cell lung cancer patients, said skilled artisan would have found it prima facie obvious to administer sotorasib in combination with the MEK inhibitor trametinib, dabrafenib and radiation therapy to treat KRAS G12C non-small cell lung cancer and KRAS G12C colorectal carcinoma patients with active brain metastases in view of Yamamoto.
Motivation to administer the MEK inhibitor trametinib, radiation therapy and dabrafenib in combination with the art-recognized KRAS G12C mutant non-small cell lung cancer and colorectal cancer treating sotorasib of Hong and Canon to KRAS G12C mutant non-small cell lung cancer and colorectal cancer patients with active brain metastases logically flows from the fact that Yamamoto teaches that trametinib, radiation therapy and dabrafenib combination is efficacious at inhibiting growth of non-small cell lung cancer patients with active brain metastasis. Considering that sotorasib is synergistic with the MEK inhibitor trametinib in reducing KRAS G12C non-small cell lung cancer and KRAS G12C colorectal tumor burden as taught by Canon, said artisan would have readily predicted that administration of the combination of sotorasib, the MEK inhibitor trametinib, radiation therapy and dabrafenib to the KRAS G12C mutant non-small cell lung cancer and colorectal cancer patients with active brain metastases would have effectively inhibited primary and metastatic tumor growth in the afflicted neoplastic patient and the active brain metastases.
Lastly, regarding Applicant’s contention that the combination of Hong, Canon and Yamamoto fail to teach the subject matter of claim 1 and that the combination of Lin and Cui fail to cure the deficiencies of Hong, Canon and Yamamoto with regards to claims 13-14, this argument is also unpersuasive. Argument directed to the combination of Hong, Canon and Yamamoto and the rejection of claims 1-12 and 15-20 have been addressed above. Regarding Applicant’s assertion that the combination of Lin and Cui fail to cure the deficiencies of Hong, Canon and Yamamoto, Applicant is reminded that it must be remembered that the references are relied upon in combination and are not meant to be considered separately as in a vacuum. It is the combination of all of the cited and relied upon references, which make up the state of the art with regard to the claimed invention. The test for obviousness is not whether the features of a secondary reference may be bodily incorporated into the structure of the primary reference and it is not that the claimed invention must be expressly suggested in any one or all of the references; but rather the test is what the combined teachings of the references would have suggested to those of ordinary skill in the art. In re Keller, 642 F.2d 413, 208, USPQ 871 (CCPA 1981). As set forth above, Lin (Lancet Oncology Vol. 16 pages 270-278. Published 2015) teaches assessment criteria for active brain metastases wherein measurable disease is defined as a contrast-enhancing lesion that can be accurately measured in at least one dimension with a minimum size of 10 mm (page 271 left col.) Lin states that for studies wherein the CNS objective response is the primary endpoint, it is highly recommended that there is a cutoff of 10 mm to limit the study to measurable disease (page 271 right col.) Meanwhile, Cui (Lung Cancer Vol. 146 pages 310-317 published 2020) teaches mutant KRAS G12C metastatic non-small cell lung cancer patients and colorectal carcinoma patients comprising active brain metastases. Cui teaches that there is a poorer prognosis in both patient classes compared to KRAS wild type tumors (pages 310-311). Cui also teaches that there is a high incidence of KRAS mutant G12C non-small cell lung cancer developing brain metastatic lesions. Cui teaches that 28% of patients diagnosed with KRAS G12C metastatic non-small cell lung cancer comprise active brain metastases and that 40% of said KRAS G12C metastatic non-small cell lung cancer patients will develop active brain metastases during follow up (page 313-314). Cui teaches that in this distinct patient population, treatments with good intracranial penetration is important for long-term disease control (page 314 right col.). As such, said artisan skilled in treating patients comprising mutant KRAS G12C non-small cell lung cancer and colorectal cancer and further comprising active brain metastases comprising administering a therapeutically effective amount of the art-recognized KRAS G12C inhibitor sotorasib in combination with trametinib, radiation therapy and dabrafenib as taught by the combination of Hong, Canon and Yamamoto above, said skilled artisan would have found it prima facie obvious to administer said sotorasib, trametinib, radiation therapy and dabrafenib therapeutic regimen to said KRAS mutant G12C non-small cell lung cancer patient or colorectal carcinoma patient with an metastatic cranial lesion of greater than 10 mm in view of Cui and Lin. Considering Lin teaches that measurable disease of an active brain metastasis is defined as a contrast-enhancing lesion that can be accurately measured in at least one dimension with a minimum size of 10 mm, said skilled artisan would have readily predicted that administering the sotorasib, trametinib and dabrafenib regimen to a patient with an active brain metastasis includes a patient with measurable disease, and thus embraces a patient with a contrast-enhancing lesion that can be accurately measured in at least one dimension with a minimum size of 10 mm. Further, considering Cui teaches that there is a high incidence of KRAS mutant G12C non-small cell lung and colorectal cancer patients developing brain metastatic lesions along with poorer prognosis of said patients compared to wild type disease, said skilled artisan would have been motivated to administer the sotorasib, trametinib and dabrafenib regimen in order to improve the therapeutic outcome in the poorer prognosed patient class.
Double Patenting-Rejection Maintained
The nonstatutory double patenting rejection is based on a judicially created doctrine grounded in public policy (a policy reflected in the statute) so as to prevent the unjustified or improper timewise extension of the “right to exclude” granted by a patent and to prevent possible harassment by multiple assignees. A nonstatutory double patenting rejection is appropriate where the conflicting claims are not identical, but at least one examined application claim is not patentably distinct from the reference claim(s) because the examined application claim is either anticipated by, or would have been obvious over, the reference claim(s). See, e.g., In re Berg, 140 F.3d 1428, 46 USPQ2d 1226 (Fed. Cir. 1998); In re Goodman, 11 F.3d 1046, 29 USPQ2d 2010 (Fed. Cir. 1993); In re Longi, 759 F.2d 887, 225 USPQ 645 (Fed. Cir. 1985); In re Van Ornum, 686 F.2d 937, 214 USPQ 761 (CCPA 1982); In re Vogel, 422 F.2d 438, 164 USPQ 619 (CCPA 1970); In re Thorington, 418 F.2d 528, 163 USPQ 644 (CCPA 1969).
A timely filed terminal disclaimer in compliance with 37 CFR 1.321(c) or 1.321(d) may be used to overcome an actual or provisional rejection based on nonstatutory double patenting provided the reference application or patent either is shown to be commonly owned with the examined application, or claims an invention made as a result of activities undertaken within the scope of a joint research agreement. See MPEP § 717.02 for applications subject to examination under the first inventor to file provisions of the AIA as explained in MPEP § 2159. See MPEP § 2146 et seq. for applications not subject to examination under the first inventor to file provisions of the AIA . A terminal disclaimer must be signed in compliance with 37 CFR 1.321(b).
The filing of a terminal disclaimer by itself is not a complete reply to a nonstatutory double patenting (NSDP) rejection. A complete reply requires that the terminal disclaimer be accompanied by a reply requesting reconsideration of the prior Office action. Even where the NSDP rejection is provisional the reply must be complete. See MPEP § 804, subsection I.B.1. For a reply to a non-final Office action, see 37 CFR 1.111(a). For a reply to final Office action, see 37 CFR 1.113(c). A request for reconsideration while not provided for in 37 CFR 1.113(c) may be filed after final for consideration. See MPEP §§ 706.07(e) and 714.13.
The USPTO Internet website contains terminal disclaimer forms which may be used. Please visit www.uspto.gov/patent/patents-forms. The actual filing date of the application in which the form is filed determines what form (e.g., PTO/SB/25, PTO/SB/26, PTO/AIA /25, or PTO/AIA /26) should be used. A web-based eTerminal Disclaimer may be filled out completely online using web-screens. An eTerminal Disclaimer that meets all requirements is auto-processed and approved immediately upon submission. For more information about eTerminal Disclaimers, refer to www.uspto.gov/patents/apply/applying-online/eterminal-disclaimer.
Claim 1-20 remain provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-4, 9-10, 30-31 of copending Application No. 18562107.
Although the claims at issue are not identical, they are not patentably distinct from each other because claims 1-4, 9-10, 30-31 of copending Application No. 18562107 are directed to treating KRAS G12C mutant non-small cell lung cancer or metastatic colorectal carcinoma comprising administering a therapeutically effective amount of sotorasib, wherein said KRAS G12C mutant cancer patient comprises active brain metastases, which overlaps with the presently claimed methodology. Claims 2-4 of copending Application 18562107 are directed to administration of doses of 960 mg/day, 480 mg/day or 240 mg/day, while claims 30-31 of copending Application 18562107are directed to wherein the patient was previously treated with at least one systemic chemotherapeutic regimen.
Applicant traverses. Applicant requests that this obvious-type double patenting rejection of record be held in abeyance until the claims of this application becomes allowable except for the obviousness-type double patenting rejection.
Response to Arguments
Applicant's arguments filed 01/20/2026 have been fully considered but they are not persuasive. As shown below, the presented claims are not found allowable. Secondly, Applicant’s statement that a terminal disclaimer will be filed when amended claims are found allowable does not comply with 37 CFR 1.111(b) (which only permits that objections and requirements as to form be held in abeyance):
37 CFR 1.111(b) states that in order to be entitled to reconsideration or further examination, the applicant or patent owner must reply to the Office action. The reply by the applicant or patent owner must be reduced to a writing which distinctly and specifically points out the supposed errors in the examiner’s action and must reply to every ground of objection and rejection in the prior Office action. The reply must present arguments pointing out the specific distinctions believed to render the claims, including any newly presented claims, patentable over any applied references. If the reply is with respect to an application, a request may be made that objections [“objections” does not include rejections] or requirements as to form not necessary to further consideration of the claims be held in abeyance until allowable subject matter is indicated. The applicant’s or patent owner’s reply must appear throughout to be a bona fide attempt to advance the application or the reexamination proceeding to final action. A general allegation that the claims define a patentable invention without specifically pointing out how the language of the claims patentably distinguishes them from the references does not comply with the requirements of this section.
In the instant case, the Applicant has failed to distinctly and specifically point out the supposed errors in the examiner’s action and failed to point out the specific distinctions between the pending claims of the instant application and claims 1-4, 9-10, 30-31 of copending Application 18562107 that make the instantly claimed patentable. The examiner notes that any future response must address the non-statutory double patenting rejection of record, either by presenting arguments why the rejection is not applicable, or by filing a terminal disclaimer over the patent. A request to hold a (full) rejection in abeyance is not permitted, and will not be considered to be in compliance with 1.111, and will not be held as a bona fide attempt to advance the application to final action.
Conclusion
In view of the rejections set forth above, no claim is allowed.
THIS ACTION IS MADE FINAL. Applicant is reminded of the extension of time policy as set forth in 37 CFR 1.136(a).
A shortened statutory period for reply to this final action is set to expire THREE MONTHS from the mailing date of this action. In the event a first reply is filed within TWO MONTHS of the mailing date of this final action and the advisory action is not mailed until after the end of the THREE-MONTH shortened statutory period, then the shortened statutory period will expire on the date the advisory action is mailed, and any nonprovisional extension fee (37 CFR 1.17(a)) pursuant to 37 CFR 1.136(a) will be calculated from the mailing date of the advisory action. In no event, however, will the statutory period for reply expire later than SIX MONTHS from the mailing date of this final action.
Any inquiry concerning this communication or earlier communications from the examiner should be directed to GEORGE W KOSTURKO whose telephone number is (571)270-5903. The examiner can normally be reached M-F 9:00-5:30.
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/GEORGE W KOSTURKO/Primary Examiner, Art Unit 1621